Suh S W, Thompson R B, Frederickson C J
Center for Biomedical Engineering, and Department of Anatomy and Neuroscience, The University of Texas Medical Branch, Galveston 77555, USA.
Neuroreport. 2001 May 25;12(7):1523-5. doi: 10.1097/00001756-200105250-00044.
The condition of status epilepticus induced by systemic administration of kainic acid (KA) causes an apparent translocation of vesicular zinc from presynaptic boutons into postsynaptic neurons. The accumulation of zinc in the somata has been identified as a contributing cause of neuronal injury. We show here that another form of status epilepticus, induced by administration of the muscarinic agonist pilocarpine, produces changes in zinc that are essentially the same as those produced by the kainic acid-induced seizures. Moreover, neurons that develop zinc staining after pilocarpine seizures are the same that shown degenerative changes. This result suggests that the loss of zinc from presynaptic boutons and the appearance of zinc in postsynaptic somata may both occur in seizures per se, regardless of etiology.
